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1 d other interventions, such as exercise, for cancer cachexia.
2 inflammation may contribute to the effect of cancer cachexia.
3 t potentially be useful for the treatment of cancer cachexia.
4 tumors, indicating a possible role of NMU in cancer cachexia.
5 it from single agent EPA in the treatment of cancer cachexia.
6  clinical states such as anorexia nervosa or cancer cachexia.
7  primary locus of neuromuscular pathology in cancer cachexia.
8 in the substantial reduction of adiposity of cancer cachexia.
9 in ligase, and its functional involvement in cancer cachexia.
10 ed peptides derived from tumors in producing cancer cachexia.
11 rexpression by tumors has been implicated in cancer cachexia.
12 addition to its previously described role in cancer cachexia.
13 ion of a glycoprotein factor associated with cancer cachexia.
14  of hepatic transcriptional reprogramming in cancer cachexia.
15 p identify potential therapeutic targets for cancer cachexia.
16 le p62 as a potential therapeutic target for cancer cachexia.
17 promising therapeutic targets for pancreatic cancer cachexia.
18  of extensor digitorum longus muscles during cancer cachexia.
19 HNC) patients are at high risk of developing cancer cachexia.
20 vel therapeutic targets by which to mitigate cancer cachexia.
21 ility as a therapeutic target, especially in cancer cachexia.
22 -6) has been long considered a key player in cancer cachexia.
23 dipose tissue wasting in the setting of PDAC cancer cachexia.
24 antagonists are actively sought for treating cancer cachexia.
25 -6, which may serve as a target for treating cancer cachexia.
26 cle in a Lewis lung carcinoma (LLC) model of cancer cachexia.
27 loss of skeletal muscle mass and function in cancer cachexia.
28 s an important role in muscle atrophy during cancer cachexia.
29 y in multiple conditions, such as ageing and cancer cachexia.
30 or of appetite suppression during pancreatic cancer cachexia.
31 trition, sarcopenia, sarcopenic obesity, and cancer cachexia.
32 -15), a circulating cytokine, is elevated in cancer cachexia.
33 , which may help develop strategies to treat cancer cachexia.
34 anisms and gaps in the knowledge surrounding cancer cachexia.
35 c deficits associated with muscle wasting in cancer cachexia.
36 y conditions, including LPS-based sepsis and cancer cachexia.
37 rward loop to regulate tumor progression and cancer cachexia.
38 fiber size in the diaphragm of patients with cancer cachexia.
39 drial assembly receptor (MasR), for treating cancer cachexia.
40  in naive conditions and in a mouse model of cancer cachexia.
41  metabolic alterations and muscle atrophy in cancer cachexia.
42 tween PDK4 and the changes in muscle size in cancer cachexia.
43 thrombosis may cause thromboinflammation and cancer cachexia.
44 reduced tolerance to chemotherapy induced by cancer cachexia.
45 nisms of immunometabolic response in AT from cancer cachexia.
46 sing therapeutic target in the management of cancer cachexia.
47 edications specifically for the treatment of cancer cachexia.
48 lammatory response during the development of cancer cachexia.
49 that IL-6 trans-signaling may be targeted in cancer cachexia.
50 thways causes skeletal muscle wasting during cancer cachexia.
51 l muscle mass in naive conditions and during cancer cachexia.
52 rcinoma (LLC) and Apc(Min/+) mouse models of cancer cachexia.
53 mass and strength and for protection against cancer cachexia.
54 rapeutic approach for at least some types of cancer cachexia.
55 es and contributes to the broader aspects of cancer cachexia.
56 is downregulated in multiple mouse models of cancer cachexia.
57 cidating the causes and treatment options of cancer cachexia.
58  such as fasting, denervation, diabetes, and cancer cachexia.
59 bo for appetite improvement in patients with cancer cachexia.
60  role in the pathogenesis of endotoxemic and cancer cachexia.
61 lpain, and caspase) in muscle wasting during cancer cachexia.
62 dramatic resistance to the muscle wasting of cancer cachexia.
63 ork for the definition and classification of cancer cachexia.
64 hypothalamic inflammatory gene expression in cancer cachexia.
65 f the ActRIIB pathway and the development of cancer cachexia.
66  approved for the prevention or treatment of cancer cachexia.
67 clinical settings, including denervation and cancer cachexia.
68  abnormalities in the liver of patients with cancer-cachexia.
69 ose tissue and skeletal muscle, hallmarks of cancer cachexia(2-4).
70 ork for the definition and classification of cancer cachexia a panel of experts participated in a for
71     Severe weight loss is characteristic for cancer cachexia, a condition that significantly impairs
72  if this molecule influences appetite during cancer cachexia, a devastating clinical entity character
73 nd, 12-week trial, we assigned patients with cancer cachexia and an elevated serum GDF-15 level (>=15
74 aling in progressive stages of clinical lung cancer cachexia and assessed whether circulating factors
75  been major advances in the understanding of cancer cachexia and asthenia.
76 pproach with combined therapy to manage both cancer cachexia and asthenia.
77 bute to impaired muscle protein synthesis in cancer cachexia and could point to novel therapeutic tar
78  urgent need for specific focus on childhood cancer cachexia and discuss potential solutions to infor
79                          Among patients with cancer cachexia and elevated GDF-15 levels, the inhibiti
80 se the underlying metabolic abnormalities of cancer cachexia and have limited long-term impact on pat
81 of PTHrP might hold promise for ameliorating cancer cachexia and improving patient survival.
82 duced in muscle in three different models of cancer cachexia and in glucocorticoid-treated mice.
83 uble lipid-mobilizing factor associated with cancer cachexia and is a novel adipokine.
84 ated with clinical and biological markers of cancer cachexia and is associated with a shorter surviva
85 al role for myostatin in the pathogenesis of cancer cachexia and link this condition to tumor growth,
86        To investigate the pathophysiology of cancer cachexia and pursue treatment options, we develop
87 ssary for normal muscle fiber atrophy during cancer cachexia and sepsis, and further suggest that bas
88 p3 and inhibited muscle fiber atrophy during cancer cachexia and sepsis.
89 ant role in muscle protein catabolism during cancer cachexia and suggest that E3alpha-II is a potenti
90 n may improve the prognosis of patients with cancer cachexia and systemic inflammation (i.e., those w
91 yeloma, rheumatoid arthritis, hypercalcemia, cancer cachexia, and Castleman's disease.
92                                              Cancer cachexia, and its associated complications, repre
93 rtant role in skeletal muscle atrophy during cancer cachexia, and more glycolytic muscles are prefere
94 ic and diet-induced metabolic dysregulation, cancer cachexia, and musculoskeletal pain.
95 necrosis factor-alpha and interleukin-6 with cancer cachexia, and the weight loss induced by leukaemi
96 tant for tumorigenicity, lung metastasis and cancer cachexia, and thus a promising therapeutic target
97 ing and pathological conditions ranging from cancer, cachexia, and diabetes to denervation and immobi
98                                              Cancer cachexia/anorexia is a complex syndrome that invo
99            Innovative approaches to treating cancer cachexia are needed.
100                    Whereas, the abundance of cancer cachexia associated bacteria, such as Dysgonomona
101 ing beneficial bacteria, and down-regulating cancer-cachexia associated bacteria.
102              These results shed new light on cancer cachexia by revealing that wasting does not resul
103          Using an established mouse model of cancer cachexia (C26 adenocarcinoma), we determined how
104 udy was to determine whether colon-26 (C-26) cancer cachexia causes diaphragm muscle fiber atrophy an
105             These data demonstrate that C-26 cancer cachexia causes profound respiratory muscle atrop
106 environments, aging, metabolism and obesity, cancer cachexia, circadian rhythms, nervous system inter
107          In models of muscular dystrophy and cancer cachexia, combined inhibition of activins and myo
108 ifactorial and early intervention to prevent cancer cachexia could take advantage of exercise, improv
109 tophagic-lysosomal proteolytic system during cancer cachexia development in humans.
110 atrophy induced by denervation as well as by cancer cachexia, diabetes, and renal failure.
111 ppears to be a promising treatment for human cancer cachexia due to its selective inhibition of p38B
112 ppears to be a promising treatment for human cancer cachexia due to its selective inhibition of p38be
113            In two different animal models of cancer cachexia, E3alpha-II was significantly induced at
114 of MeAT from patients and an animal model of cancer cachexia enabled us to identify early disruption
115 oxidation in tumor-bearing mice and prevents cancer cachexia, even under calorie-restricted condition
116               With no effective treatment of cancer cachexia, future therapies directed at preserving
117                       Experimental models of cancer cachexia have indicated that systemic inflammatio
118 mmobilization, aging, catabolic steroids, or cancer cachexia, however, are poorly understood.
119 cytokines have been shown to be mediators of cancer cachexia; however, the role of cytokines in dener
120 n1/MAFbx and muscle wasting are hallmarks of cancer cachexia; however, the underlying mechanism is un
121        Moreover, depletion of TRAF6 prevents cancer cachexia in an experimental mouse model.
122            Clinical care and research around cancer cachexia in children is lacking.
123 , is a critical mediator of IL-6 function in cancer cachexia in male mice.
124 t of skeletal muscle wasting associated with cancer cachexia in mouse models and in patients with can
125 SS2 on the nonselective macropinocytosis and cancer cachexia in pancreatic cancer remains elusive.
126 anations include negative effects related to cancer cachexia in patients with low BMI, increased drug
127 uce phenotypes identified in mouse models of cancer cachexia, including muscle fiber atrophy, sarcole
128  roles in tumor-induced systemic wasting and cancer cachexia, including muscle wasting and lipid loss
129                                  In summary, cancer cachexia increases EcSOD expression in extensor d
130 P mice die within 6 weeks of age from severe cancer cachexia induced by large, activin-secreting ovar
131 the IKK complex are cardioprotective against cancer cachexia-induced cardiac atrophy and systolic dys
132 peutic potential of p62 and Nrf2 to mitigate cancer cachexia-induced muscle atrophy.
133 g pathway downstream of IL-1beta to mitigate cancer cachexia-induced muscle atrophy.
134  phenotype of muHuR-KO mice protects against cancer cachexia-induced muscle loss.
135                                              Cancer cachexia involves the loss of weight, mainly in s
136                                              Cancer cachexia is a common, debilitating condition with
137                                              Cancer cachexia is a complex metabolic condition charact
138                                              Cancer cachexia is a complex systemic wasting syndrome.
139                    Muscle protein wasting in cancer cachexia is a critical problem.
140                                              Cancer cachexia is a devastating metabolic syndrome char
141                                              Cancer cachexia is a highly prevalent condition associat
142                                              Cancer cachexia is a life-threatening syndrome that affe
143                                              Cancer cachexia is a major cause of patient morbidity an
144                                              Cancer cachexia is a multifactorial syndrome characteriz
145                                              Cancer cachexia is a multifactorial syndrome characteriz
146                                              Cancer cachexia is a multifactorial syndrome characteriz
147                                              Cancer cachexia is a multifactorial syndrome involving m
148                                              Cancer cachexia is a multifactorial syndrome that is poo
149                                              Cancer cachexia is a severe wasting syndrome characteriz
150                                              Cancer cachexia is a syndrome of progressive wasting whi
151                                              Cancer cachexia is a systemic metabolic syndrome charact
152                                              Cancer cachexia is an unmet medical need and our data su
153                                              Cancer cachexia is characterized by a continuous loss of
154                                              Cancer cachexia is characterized by reductions in periph
155                                              Cancer cachexia is mediated in part by TNF-alpha.
156 has characterized skeletal muscle wasting in cancer cachexia, limited studies have investigated how c
157 es to levels approximating those observed in cancer cachexia models induced a more rapid and profound
158                                           In cancer cachexia models, maintaining skeletal muscle expr
159                Here, we show that in several cancer cachexia models, pharmacological blockade of ActR
160 he liver in various weight-stable cancer and cancer cachexia models.
161 lly, we observed that in an in vivo model of cancer cachexia, Mstn expression coupled with downregula
162                                           In cancer cachexia, muscle depletion is related to morbidit
163  contributes to peripheral tissue wasting in cancer cachexia, offering perspectives for future therap
164 abel, phase 1b study involving patients with cancer cachexia, ponsegromab, a humanized monoclonal ant
165                We tested the hypothesis that cancer cachexia progression would induce oxidative post-
166 use and cellular models, we demonstrate that cancer cachexia promotes muscle EcSOD protein expression
167                   However, the mechanisms of cancer cachexia remain poorly understood.
168                                              Cancer cachexia remains a largely intractable, deadly co
169               The role of hypermetabolism in cancer cachexia remains unclear.We studied the relation
170 d in various biological functions, including cancer cachexia, renal and heart failure, atherosclerosi
171 cle during systemic wasting states (fasting, cancer cachexia, renal failure, diabetes).
172 ved kinase inhibitor, nilotinib, ameliorates cancer cachexia, representing a potential therapeutic st
173 ved kinase inhibitor, nilotinib, ameliorates cancer cachexia, representing a potential therapeutic st
174 of LCN2 in the central nervous system, while cancer cachexia results in a distribution specific to th
175 ogenesis in a plethora of diseases including cancer cachexia, sarcopenia, and muscular dystrophy.
176 from the tumor, phenotypes that resemble the cancer cachexia seen in human patients.
177  rule pathway, the same pathway activated in cancer cachexia, sepsis, and hyperthyroidism.
178 red muscles from fasted mice, from rats with cancer cachexia, streptozotocin-induced diabetes mellitu
179 rnover induces immunometabolic modulation in cancer cachexia syndrome.
180  skeletal muscle wasting in murine models of cancer cachexia that is disrupted in skeletal muscle of
181                                 In mice with cancer cachexia, the MasR agonist AVE 0991 slowed tumor
182                                           In cancer cachexia, the presence of a tumor triggers system
183                                In a model of cancer cachexia, they significantly reduce muscle atroph
184 d (ii) a 3D microphysiological model of lung cancer cachexia to study inflammatory and oxidative musc
185                                              Cancer cachexia was defined as a multifactorial syndrome
186  Here, using a Lewis lung carcinoma model of cancer cachexia, we show that tumour-derived parathyroid
187             Using this model, and a model of cancer cachexia, we test the hypothesis that CD4(+)CD44(
188 bute to increased muscle proteolysis in lung cancer cachexia, whereas the absence of downstream chang
189 undescribed mechanism for the development of cancer cachexia, whereby progressive MDSC expansion cont
190 served in patients and in animal models with cancer cachexia, which may contribute to cachexia pathop
191 ism is a promising new approach for treating cancer cachexia, whose inhibition per se prolongs surviv

 
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